The previously known effects of boron on animal metabolism have been reviewed by Nielsen ["Trace Elements in Human and Animal Nutrition," Vol. 2, pp. 422-427, Academic, New York (1986)].
In 1981, Hunt and Nielsen [In "Trace Element Metabolism in Man and Animals-4," pp. 597-600, Aust. Acad. Sci., Canberra (1981)]reported that boron deprivation depressed growth and elevated alkaline phosphatase activity in chicks fed inadequate cholecalciferol. Cholecalciferol deficiency enhanced the need for boron, and it was postulated that boron might interact with the metabolism of calcium, phosphorus, or magnesium.
Further experiments suggested that the influence of boron was the result of altered parathormone activity [F. H. Nielsen, In "Trace Elements in Man and Animals-5 Abstracts," p. 26, Aberdeen, Scotland (1984)]. This hypothesis was also supported by Elsair et al. [Fluoride 15: 30-38 (1980)], who reported that high dietary boron partially alleviated the fluoride-induced secondary hyperparathyroid signs of hypercalcemia in rabbits.
Further indications of a relationship between boron and calcium are that boron or boron compounds can influence calcium metabolism and that boron levels change in animals with abnormal calcium metabolism. Amine cyanoboranes and amine carboxyboranes effectively block induced arthritis [I. H. Hall et al., J. Pharm. Sci. 69: 1025-1029 (1980)], and tablets containing magnesium carbonate and sodium borate have been sold as a remedy for arthritis. This effect was thought to be attributable to changed ATP metabolism at the cell membrane level to cause cell division and regeneration [R. E. Newnham, In "Trace Element Metabolism in Man and Animals-4," pp. 400-402, Aust. Acad. Sci. Canberra (1981)].
Estrogens are known to exert profound effects on the metabolism of calcium and phosphorus as well as lipids and proteins in the human body. Administration of estrogen hormones in man decreases the level of circulating blood lipids; this effect has drawn attention to a possible role of sex hormones in atherosclerosis.
Estrogen therapy is used to alleviate the symptoms of bone decalcification seen in postmenopausal osteoporosis. However, prolonged estrogen administration may result in elevation of serum calcium and phosphate levels, with calcification and hyperossification of the long bones, so that the marrow cavity may disappear and result in anemia. [See A. White et al., "Principles of Biochemistry," McGraw-Hill, New York, p. 858 (1964).]